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NFAT3 transcription factor inhibits breast cancer cell motility by targeting the Lipocalin 2 gene.

By Marjorie Fougère, Benoît Gaudineau, Jérome Barbier, Frédéric Guaddachi, Jean-Paul Feugeas, Didier Auboeuf and Sébastien Jauliac


International audienceNFAT1 and NFAT5 act as pro-invasive and pro-migratory transcription factors in breast carcinoma, contributing to the formation of metastases. We report that NFAT3 is specifically expressed in estrogen receptor alpha positive (ERA+) breast cancer cells. We show that NFAT3 inhibits by itself the invasion capacity of ERA+ breast cancer cells and needs to cooperate with ERA to inhibit their migration. Conversely, NFAT3 downregulation results in actin reorganization associated with increased migration and invasion capabilities. NFAT3 signaling reduces migration through inhibition of Lipocalin 2 (LCN2) gene expression. Collectively, our study unravels an earlier unknown NFAT3/LCN2 axis that critically controls motility in breast cancer

Topics: NFAT3, LCN2, estrogen receptor alpha, motility, breast, MESH : Actins, MESH : Acute-Phase Proteins, MESH : Neoplasm Invasiveness, MESH : Protein Binding, MESH : Proto-Oncogene Proteins, MESH : Breast Neoplasms, MESH : Cell Line, Tumor, MESH : Cell Movement, MESH : Estrogen Receptor alpha, MESH : Gene Expression Regulation, Neoplastic, MESH : Humans, MESH : Lipocalins, MESH : NFATC Transcription Factors, [ SDV.CAN ] Life Sciences [q-bio]/Cancer
Publisher: Nature Publishing Group
Year: 2010
DOI identifier: 10.1038/onc.2009.499
OAI identifier: oai:HAL:inserm-00541837v1
Provided by: Hal-Diderot
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